Critical Realism and Epilepsy-related QofL

By | November 21, 2012

This blog builds on my previous precis of basic critical realism to offer an illustration of its potential for coming to terms with ‘interdisciplinarity’. The focus is on epilepsy-related quality of life, and my analysis draws on work conducted with Caroline Selai and Panagiota Afentouli and published as a chapter in a volume edited by Sasha Scambler and I entitled ‘New Directions in the Sociology of Chronic and Disabling Conditions’ (Palgrave Macmillan, 2010.

The concept of epilepsy-related quality of life (ERQOL) is a contested one. While some insist that there can be ‘objective’ markers of ERQOL, others argue that it is an inherently ‘subjective’ notion. Clearly objective and subjective ERQOL need not correspond: epilepsy pursuant on severe brain injury might by common consent be associated with poor objective ERQOL without this translating into a poor subjective ERQOL. Clinicians and life and social scientists are likely to agree, however, that biological, psychological and social mechanisms have a potential bearing on both objective and subjective ERQOL, even if they are likely to go on to diverge on appropriate interventions.

The causal history of ERQOL can be extremely complex. For example, deleterious effects of epilepsy can be felt in the absence of any salient biological structures or mechanisms. This is likely to occur when epilepsy is misdiagnosed: application of the diagnostic label can itself – by authoritatively foisting a new, unwelcome and stigmatising social identity on the person-cum-patient – trigger psychological and/or social mechanisms to negative effect. If on the other hand epilepsy is but one symptom of a particularly severe underlying pathology, biological mechanisms can cancel out or override the causal potential of psychological and social mechanisms (Sasha Scambler has shown this in relation to the rare juvenile Batten disease for example). Genetic predisposition and brain insult can also be mediated by psychological mechanisms that over time ‘decide’ ERQOL. The causal efficacy of psychological mechanisms like internal versus external locus of control can themselves be dependent on contexts shaped by social mechanisms, or, for that matter, contingent happenings or agency.

What these varied scenarios commend is scientific caution. Biological, psychological and social structures and mechanisms can vary in their causal efficacy from individual to individual as well as by social or cultural context. Moreover they can and frequently do interact: one genus, acting upstream or downstream, can ‘cancel out’ or ameliorate the impact of others. Critical realism, in my view, allows for this fluidity. To better appreciate why calls for some conceptual refinement. Danermark et al (2002: 55) do this splendidly:

‘The objects have the powers they have by virtue of their structures, and mechanisms exist and are what they are because of this structure; this is the nature of the object. There is an internal and necessary relation between the nature of an object and its causal powers and tendencies. This can also be expressed as follows (Collier, 1994:43): ‘things have the powers they do because of their structures … Structures cause powers to be exercised, given some input, some ‘efficient cause’, eg the match lights when you strike it’). This in turn is an example of a mechanism having generated an event. A mechanism is that which can cause something in the world to happen, and in this respect mechanisms can be of many different kinds’ (Danermark et al: ‘Explaining Society’, Routledge, 2002; Collier: Critical Realism, Verso, 1994).   

So a generative mechanism operates when it is being triggered. Unlike the internal and necessary relation between objects and their causal powers, however, the relation between causal powers or mechanisms and their effects is external and contingent. The reason for this is that, underlying phenomena in the domain of the actual, there are many biological, psychological and social mechanisms that are concurrently active. Thus ERQOL is a complex effect of influences emanating from an array of multi-level mechanisms, where some mechanisms reinforce while others frustrate others. Danermark et al (2002: 56) again:

‘Taken together this – that objects have powers whether exercised or not, mechanisms exist whether triggered or not and the effects of the mechanisms are contingent – means we can say that a certain object ‘tends’ to act or behave in a certain way’. 

Thus numerous and fortuitous circumstances can play their part in determining whether a specific causal power will manifest itself or not.

So one lesson for sociologists, if they ever doubted it, is that ERQOL cannot be understood or explained solely in terms of social mechanisms governing context (although sociology can make its own discrete and irreducible contribution). Not only do biological mechanisms typically matter, but psychological mechanisms typically condition people’s handling of biologically-induced ‘impairment effects’ (as Carol Thomas calls them) in socially-induced contexts. Further complications arise with unannounced contingency in human affairs and the play of human reflexivity and agency. In short, sociology’s research programmes on ERQOL only tell part of the story. And even genuinely interdisciplinary (biological + psychological + social) research programmes would not tell the whole story: the explanatory power generated would not be matched by an equivalent predictive power: people and their circumstances can and do defy science.

Critical realism in this connection has a threefold return. First, it recognises and allows for an adequate ontology of objects, powers/mechanisms and tendencies in open systems, and does so without falling foul of the naturalistic fallacy (namely, some form of reductionism). Second, it requires and facilitates a move beyond the ubiquitous positivistic pursuit of statistically significant associations between variables, be they biological, psychological or social or, more rarely, some combination of these. And third, it calls for methodological rigour even as it denounces positivist ‘textbook’ emphases on measurement via operationalisation and quantification using ever more advanced forms of multivariate analysis. The denunciation is not of these positivist accessories per se, but rather of the underlying assumption that phenomena can be predicted, and therefore explained, given ’empirical’ study of the ‘actual’, that is, without resort to Bhaskar’s ‘real’. The potential for experimental closure in open systems is exaggerated.

It does not follow from this advocacy of a critical realist frame that extant positivist research – quantitative, but qualitative as well -is redundant. These findings are grist to the mill, as ‘cues, in that they often favour particular retroductive/abductive inferences to ‘real objects and their causal powers/generative mechanisms and tendencies. Moreover more than science is at stake. Much research is driven by an instrumental concern to improve objective/subjective ERQOL. In this vein I end with a paragraph or two on pointers towards an intervention model. It arises out of my earlier hidden distress model of epilepsy (see my Epilepsy, Tavistock, 1989).

Using the shorthand of this blog, the hidden distress model acknowledges that biological mechanisms, extending from genetics to the neuropharmacology of anti-epileptic drugs, typically matter in relation to ERQOL, deeper understanding often mitigating epilepsy’s assault on people’s day-to-day lives via more effective treatment. But even severe biological assaults ‘may not’ be decisive for ERQOL. Psychological mechanisms typically condition people’s handling of epilepsy’s assault, and therefore its impact on ERQOL, independently of its biological severity or intractability. There is considerable scope for counselling, targeting the interface between enduring psychological traits and coping styles. Yet psychological mechanisms too ‘may not’ be decisive for ERQOL. Social mechanisms typically provide people with contexts, some of which prove decisive for ERQOL. Spontaneous reactions to a witnessed seizure can be pivotal in the long as well as the short term. Social mechanisms too ‘may not’ be compelling for ERQOL.

In line with the hidden distress model, which accorded primary significance to felt stigma and a concomitant urge to fearful secrecy and compromised aspiration, it might be suggested that what I will call, after Bourdieu, an epilepsy habitus is key. This refers to an enduring, context-induced mindset, with felt stigma at its core, which predisposes to acquiescence or passivity with regard to socially disadvantaging difference. Anticipating discrimination (enacted stigma), people with epilepsy often (learn to) do to themselves what they anticipate others will ‘inevitably’ do to them. An epilepsy habitus can form independently of either biological or psychological tendencies, although it too may lose relevance for ERQOL, for example in the presence of prepotent biological mechanisms (eg severe brain injury). Clinical and public health interventions might reasonably aim to prevent the development/grip of an epilepsy habitus.

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